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Metabolic Needs (metabolic + need)
Selected AbstractsSmall-for-size liver syndrome after auxiliary and split liver transplantation: Donor selectionLIVER TRANSPLANTATION, Issue 9 2003Nigel Heaton Small-for-size liver grafts can be defined by a recognizable clinical syndrome that results from the transplantation of too small a functional mass of liver for a designated recipient. A graft to recipient body weight ratio less than 0.8, impaired venous inflow, and enhanced metabolic demands in patients with poor clinical conditions must be considered as main factors leading to the small-for-size syndrome (SFSS) when using living and cadaveric partial grafts such as split and auxiliary liver grafts. Increased risk of graft dysfunction is currently observed in fatty infiltration of more than 30%, abnormal liver test results (especially bilirubin and gamma glutaryl transferase), and other donor risk factors such as high inotrope administration and donor stay in the intensive care unit (>5 days). Older donors are especially vulnerable to prolonged cold ischemia and high inotrope levels, giving rise to early graft dysfunction and prolonged cholestasis. Increased metabolic need on a functionally small-for-size graft predisposes to surgical and septic complications and poorer survival. Splitting livers into right and left lobe grafts increases the potential risk of small-for-size grafts for both recipients. Several techniques of venous outflow reconstruction/implantation have been proposed to reduce the risk of obstruction postoperatively. Prevention and management of SFSS will improve in parallel with the increased experience, allowing us optimum usage of available organs and reducing overall morbidity and mortality. (Liver Transpl 2003;9:S26-S28.) [source] Ocular blood flow autoregulation and the clinical implications of its alterationACTA OPHTHALMOLOGICA, Issue 2009G GARHOFER Autoregulation is commonly defined as the ability of a vascular bed to adapt blood flow to changes in ocular perfusion pressure (pressure autoregulation) or to adapt to changes in metabolic need (metabolic autoregulation). Considering the high metabolic turnover of the eye, its intact function is strongly dependent on a stable blood supply, assured by an intact vascular autoregulation. However, it has been shown that in the recent years that several ocular diseases such as glaucoma, diabetic retinopathy or age related macula degeneration are associated with an impaired autoregulation. This vascular dysregulation may lead to an under- or overperfusion of the tissue and in turn to ischemia and/or oxidative stress. This talk seeks to summarize our current knowledge of autoregulation in the ocular vascular beds. Furthermore, the possible reasons of impaired autoregulation and how this may relate to ocular pathologies will be discussed. [source] The relationship between peripheral glucose utilisation and insulin sensitivity in the regulation of hepatic glucose production: studies in normal and alloxan-diabetic dogsDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2006M. J. Christopher Abstract Background Hepatic glucose overproduction (HGP) of diabetes could be primary or could occur in response to the metabolic needs of peripheral (skeletal muscle (SkM)) tissues. This question was tested in normal and diabetic dogs. Methods HGP, SkM glucose uptake (Rdtissue), metabolic clearance of glucose (MCRg) and glycolytic flux (GFexog), and SkM biopsies were measured in the same dogs before and after alloxan-induced diabetes. Normal dogs were exposed to (1) an extended 20-h fast, (2) low- and high-dose glucose infusions (GINF) at basal insulinaemia, and chronic diabetic dogs were exposed to (3) hyperglycaemia, (4) phlorizin-induced normoglycaemia, and (5) poor and good diabetic control. Results (1) Prolonged fast: HGP, Rdtissue, and GFexog fell in parallel (p < 0.05). (2) Low-dose GINF: plasma glucose, insulin, Rdtissue, MCRg, and GFexog were unchanged, but HGP fell by ,40%, paralleling the supplemental GINF. (3) High-dose GINF at basal insulin: plasma glucose doubled and synchronous changes in HGP, Rdtissue, MCRg, and GFexog occurred; ICglucose, G6P, and glycogen were unchanged. (4) Hyperglycaemic diabetes: HGP was raised (p < 0.05), matching urinary glucose loss (UGL) and decreased MCRg, and maintaining normal basal Rdtissue and GFexog. SkM ICglucose was increased and glycogen decreased (both p < 0.05). (5) Phlorizin-induced normoglycaemia in diabetic dogs: HGP rose, matching the increased UGL, while maintaining normal Rdtissue and GFexog. Intramuscular substrates normalised. (6) Whole body and SkM metabolism normalised with correction of the insulin resistance and good diabetic control. Conclusion HGP reflects whether SkM is in a state of relative glucose ,excess' or absolute/relative glucose ,deprivation'. Copyright © 2005 John Wiley & Sons, Ltd. [source] Absence of phosphoglucose isomerase-1 in retinal photoreceptor, pigment epithelium and Muller cellsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2004Simon N. Archer Abstract Macroarray analysis was used to compare equal amounts of cDNA from wild-type and rd/rd (retinal degeneration) mice, collected at P90 when photoreceptor degeneration is virtually complete. A stronger signal for the glycolytic enzyme phosphoglucose isomerase (Gpi1) was observed in the rd/rd sample. Extracellularly, Gpi1 may act as a cytokine, independently described as neuroleukin and autocrine motility factor. Retinal Gpi1 expression was investigated by Northern and Western blot analysis and immunohistochemistry. Double-labelling was performed with antibodies against Gpi1 and calbindin-D, glutamine synthetase, RPE65, calretinin and ultraviolet opsin in order to provide positive cell type identification. Northern and Western blots showed double expression levels per microgram of RNA and protein, respectively, in the rd/rd retina compared with wild-type. However, the total amount of Gpi1 protein per retina was indistinguishable. Gpi1 immunoreactivity was found in ganglion, amacrine, horizontal and bipolar cells, but not in rods, cones, pigment epithelium and Muller cells. This distribution explains why the absolute amounts of Gpi1 protein were not appreciably different between wild-type and the rd/rd phenotype, where rods and cones are absent, whilst the relative contribution of Gpi1 to the total protein and RNA pools differed. Some extracellular immunoreactivity was observed in the photoreceptor matrix around cones in freshly fixed tissue only, which could possibly reflect a role as a cytokine. We propose that glycolysis in Gpi1-negative cells proceeds entirely through the pentose phosphate pathway, creating NADPH at the cost of organic carbon. We hypothesize that the unique metabolic needs of photoreceptors justify this trade-off. [source] Living on the edge: feeding of subtropical open ocean copepodsMARINE ECOLOGY, Issue 2 2006Gustav-Adolf Paffenhöfer Abstract The objective of this study was to provide quantitative information on environmental feeding rates of warm water oceanic epipelagic copepods. We determined clearance rates at 23 °C for various particle size ranges in shipboard studies in the western oligotrophic subtropical Atlantic Ocean for females of the calanoid species Clausocalanus furcatus and Mecynocera clausii. These in situ clearance rates were then applied to the various particle size ranges of environmental particle spectra of auto- and heterotrophs at different depths from three stations in the western Atlantic. After calculating the metabolic demands of each of these two copepod species and applying an assimilation efficiency of 90%, we determined that C. furcatus meets its metabolic demands in all six cases, and M. clausii in two of six cases. Clausocalanus furcatus would also meet its energy demands at 25 °C, where it is often found, while M. clausii at 20 °C, where it is regularly found, would cover its metabolic needs in four of six cases. It is hypothesized that these species, and most likely most of the other co-occurring copepod species, are limited in their abundance by food availability, or, better said, are ,living on the edge' in relation to food abundance. [source] Seasonal changes in female size and its relation to reproduction in the parasitoid Asobara tabidaOIKOS, Issue 2 2001Jacintha Ellers The relation between female size and fitness was studied in female Asobara tabida throughout the field season. The size of A. tabida females varied considerably, with average size being smallest in the middle of the season. There was a positive correlation of realized fecundity with size, and the fitness advantage of larger females increased later in the season. A possible explanation for this can be found in the energy expenditure during the season. Regression analysis showed that fat use increases with size of the female, but also with temperature. Temperature was low early and late in the season, but high in the middle. We argue that the high temperatures may constrain fitness advantages of large females because of their increased metabolic needs. Variation in the form of the fitness function within the season may moderate directional selection for larger females. [source] Functional genomics of phosphate antiport systems of plastidsPHYSIOLOGIA PLANTARUM, Issue 4 2003Ulf-Ingo Flügge Plant cells require a co-ordination of metabolism between their major compartments, the plastids and the cytosol, in particular as certain metabolic pathways are confined to either compartments. The inner envelope membrane of the plastids forms the major barrier for metabolite exchange and is the site for numerous transport proteins, which selectively catalyse metabolite exchanges characteristic for green and/or non-green tissues. This report is focused on the molecular biology, evolution and physiological function of the family of phosphate translocators (PT) from plastids. Until now, four distinct subfamilies have been identified and characterized, which all share inorganic phosphate as common substrate, but have different spectra of counter exchange substrates to fulfil the metabolic needs of individual cells and tissues. The PTs are named after their main transported substrate, triose phosphate (TPT), phosphoenolpyruvate (PPT), glucose 6-phosphate (GPT) and xylulose 5-P (XPT). All PTs belong to the TPT/nucleotide sugar transporter (NST) superfamily, which includes yet uncharacterized PT homologues from plants and other eukaryotes. Transgenic plants or mutants with altered transport activity of some of the PTs have been generated or isolated. The analysis of these plant lines revealed new insights in the co-ordination and flexibility of plant metabolism. [source] Mechanisms by which systemic salbutamol increases ventilationRESPIROLOGY, Issue 2 2006Antony E. TOBIN Background and objective: Salbutamol (SAL) has systemic effects that may adversely influence ventilation in asthmatic patients. The authors sought to determine the magnitude of this effect and mechanisms by which i.v. SAL affects ventilation. Methods: A prospective study of nine healthy subjects (eight men, one woman; age 23 ± 1.4 years (SD)) was undertaken. Each subject received i.v. SAL at 5, 10 and 20 µg/min each for 30 min at each dose and was observed for 1 h post infusion. Minute ventilation (V,E), oxygen consumption (V,O2), CO2 production (V,CO2), occlusion pressure (P0.1), heart rate, blood pressure, respiratory rate, glucose, arterial blood gases, lactate and potassium (K+) were recorded at baseline and at 30-min intervals. The effect of 100% oxygen on V,E and P0.1 during SAL infusion at 20 µg/min was observed. Results are expressed as mean ± SEM. Results: V,E was significantly increased at 20 µg/min SAL (37.8 ± 12.1%, P = 0.01), as were V,O2 (22.5 ± 5.1%, P < 0.01) and V,CO2 (40.9 ± 10.6%, P < 0.01). Ventilation was in excess of metabolic needs as demonstrated by a rise in the respiratory exchange ratio (0.87 ± 0.03 to 0.99 ± 0.04, P < 0.05). Serum lactate rose by 124 ± 30.4% from baseline to 20 µg/min (1.1 ± 0.1 to 2.3 ± 0.25 mmol/L, P < 0.01) and base excess decreased (0.89 ± 0.56 to vs. ,1.75 ± 0.52 mmol/L, P < 0.01) consistent with a lactic acidosis contributing to the excess ventilation. There was no significant differences in V,E or P0.1 with FIO2 = 1.0, suggesting peripheral chemoreceptor stimulation was not responsible for the rise in V,E. At 20 µg/min SAL, K+ fell significantly from baseline (3.8 ± 0.06 to 2.8 ± 0.09 mmol/L, P < 0.001). Conclusion: Systemic SAL imposes ventilatory demands by increasing metabolic rate and serum lactate. This may adversely affect patients with severe asthma with limited ventilatory reserve. [source] Bone Remodeling in Maxilla, Mandible, and Femur of Young DogsTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2008Sarandeep S. Huja Abstract Bone remodeling in the jaw is essential for metabolic needs, mechanical demands and for growth of the skeleton. Currently, there is no information on remodeling in the jaw of young dogs. Four ,5-month-old male dogs were given a pair of calcein bone labels. After killing, bone sections were obtained from the maxilla, mandible, and femur. The jaw specimens were obtained from regions associated with erupting permanent teeth. Undecalcified specimens were prepared for examination by histomorphometric methods to evaluate mineral apposition rate (,m/d), mineralizing surface/bone surface (%), and bone formation rate (BFR, %/yr) in the bone supporting erupting teeth and in the femurs. Only intracortical secondary osteonal remodeling units were measured. There were significant (P < 0.05) differences in the BFR for the three sites examined, with the highest BFR (72%/yr) being in the femur. The mandible had a BFR twofold greater than the maxilla (51%/yr vs. 25.5%/yr). The rate of turnover in the jaw and femur of young dogs is distinct from a similar comparison between the jaw and appendicular skeleton of adult (,1 yr old) dogs. Although BFR decreases with age in the femur, it remains elevated in the jaws. Anat Rec, 291:1,5, 2007. © 2007 Wiley-Liss, Inc. [source] Role of leptin in the regulation of growth and carbohydrate metabolism in the ovine fetus during late gestationTHE JOURNAL OF PHYSIOLOGY, Issue 9 2008Alison J. Forhead Leptin is an important regulator of appetite and energy expenditure in adulthood, although its role as a nutritional signal in the control of growth and metabolism before birth is poorly understood. This study investigated the effects of leptin on growth, carbohydrate metabolism and insulin signalling in fetal sheep. Crown,rump length-measuring devices and vascular catheters were implanted in 12 sheep fetuses at 105,110 days of gestation (term 145 ± 2 days). The fetuses were infused i.v. either with saline (0.9% NaCl; n= 6) or recombinant ovine leptin (0.5,1.0 mg kg,1 day,1; n= 6) for 5 days from 125 to 130 days when they were humanely killed and tissues collected. Leptin receptor mRNA and protein were expressed in fetal liver, skeletal muscle and perirenal adipose tissue. Throughout infusion, plasma leptin in the leptin-infused fetuses was 3- to 5-fold higher than in the saline-infused fetuses, although plasma concentrations of insulin, glucose, lactate, cortisol, catecholamines and thyroid hormones did not differ between the groups. Leptin infusion did not affect linear skeletal growth or body, placental and organ weights in utero. Hepatic glycogen content and activities of the gluconeogenic enzymes glucose-6-phosphatase and phosphoenolpyruvate carboxykinase in the leptin-infused fetuses were lower than in the saline-infused fetuses by 44, 48 and 36%, respectively; however, there were no differences in hepatic glycogen synthase activity or insulin signalling protein levels. Therefore, before birth, leptin may inhibit endogenous glucose production by the fetal liver when adipose energy stores and transplacental nutrient delivery are sufficient for the metabolic needs of the fetus. These actions of leptin in utero may contribute to the development of neonatal hypoglycaemia in macrosomic babies of diabetic mothers. [source] | ||||||||||||||||||||||